Treatment goals for HTN therapy
ultimate goal is to reduce morbidity/mortality
Dietary Approaches to Stop HTN, low fat, low sodium, can reduce BP up to 8-14mmHg
Lifestyle modifications for reducing BP
DASH diet, weight loss (apple vs pear shape, BMI >27=increased BP), smoking cessation (reduces BP in 20-30mins), alcohol restriction(2/day men, 1/day women, can reduce BP by 2-4mmHg), sodium restriction (<2.4grams/day, can reduce BP by 2-8mmHg), physical activity (30mins aerobic on most days, can reduce BP by 4-9mmHg), biofeedback/relaxation, caffeine reduction
T or F: all BP drugs reduce the BP by the same amount
TRUE: all BP meds give about the same result, therapy choice is made by concurrent medical conditions and drug treatments, SE profile, cost, demographics, previous drug therapy failures
Initial drug choice for ppl with stage 1 HTN and no compelling indications
thiazide diuretics are first line. may add ACEI, ARB or CCB or any combo
intial drug choice for ppl with stage 2 HTN and no compelling indications
two drug combo, usually includes a thiazide diuretic and either ACEI, ARB or CCB
treatment choice for pt with HTN and left ventricular dysfunction
First line: diuretic and ACEI then add B blocker. Second line: ARB or aldosterone antagonist
treatment choice for pt with HTN and post MI
First line: B blocker then ACEI or ARB. Second line: aldosterone antagonist
treatment choice for pt with HTN and coronary disease
First line: B blocker then ACEI or ARB. Second line: CCB or diuretic
treatment choice for pt with HTN and diabetes
First line: ACEI or ARB. Second line: diuretic. Third line: B blocker, CCB
treatment choice for pt with HTN and chronic kidney disease
ACEI or ARB
treatment choice for pt with HTN and recurrent stroke prevention
diuretic + ACEI or ARB
how often should K and Creat be taken for pts on HTN therapy
how often should patients be seen if their BP is not yet stable
how often should patients be seen if they have reached their BP goal and are stable
Q 3-6 months
the main antihypertensive drugs
Diuretics (thiazides and loop), ACEI/ARB, CCB, B blockers, peripheral alpha blockers
drug of choice for HTN, MOA=inhibits NA reabsorption in distal tubule thereby increasing H2O and NA excretion which leads to decreased blood volume, they also do have some indirect vasodilation long term, 3-4 wks for full effect, ppl with CrCL<30 will not have response (except for metolazone)
HCTZ(12.5-25mg daily), chlorthalidone (12.5-25mg daily), metolazone(2.5-5mg daily, ok for renal pts), indapamide(1.25-2.5mg daily, neutral lipid effects)
drug of choice for renal insufficiency and CHF, MOA=inhibits Na reabsorption in the Loop of Henle and causes some vasodilation long term,
Loop diuretic agents
furosemide, bumetanide, torsemide
K sparing diuretics
drug of choice for those that experienced hypokalemia, MOA depend on agent
K sparing diuretic agents
Triamterene/amiloride MOA=inhibits Na reabsorption in the collecting duct thru the Na/K ATPase pump, Spironolactone/eplerenone MOA=aldosterone receptor antagonist (more potent then triam/amil but slower onset of action
adverse effects of diuretics
Hypokalemia (<3.5 tx is supplement), hyperuricemia, hypercalcemia (thiazides), glucose intolerence (thiazides >25mg), photosensitivity, hyponatremia, hypomagnesemia, hypochloremia, hyperkalemia (K sparing/ACEI/K supplement), increased LDL and triglycerides (not indapamide), sex dysfunction, orthostatic hypotension, gynecomastia (spironolactone)
which diuretic is preferred for most patients according to JNC7?
which antihypertensive is preferred in African Americans and why?
diuretics work well because African Americans tend to have decreased renins which cause blood volume dependent HTN
which diuretic is preferred in patients with CrCL <30mL/min?
avoid thiazide and K sparing, use loop and metolazone
which diuretic has a benefit for osteoporosis?
thiazides because they slow bone demineralization
T or F: diuretics can cause lithium toxicity
TRUE kidneys will hold on to lithium in place of Na
what should be monitored while a patient is on diuretic therapy?
BP, renal function, electolytes, glucose, uric acid
Patient education points about diuretics include....
take in AM, if BID take 2nd dose in afternoon, watch for muscle cramps/weakness
K rich foods (dried fruit, bannana, cantaloupe, orange juice, cooked spinach, potatoes), salt substitutes (Mrs. Dash or Mortons) KCl supplements
Angiotensin Converting Enzyme Inhibitors (ACEI) MOA
MOA=blocks ACE which decreases angiotensin II which causes vasodilation, decreases ADH, decreases LVH effects and decreases aldosterone also ACEI inhibit the kinase enzyme which causes an increase in bradykinins which causes vasodilation and cough
What are the ACEI agents?
enalapril, ramipril, moexipril, benazepril, quinapril, lisinopril, trandolapril, perindopril, fosinopril (dual metabolism), captopril (HTN urgency)
Angiotensin II Receptor Blockers (ARBs) MOA
MOA=inhibit angiotensin II receptors, no effect on bradykinins so no cough
What are the ARB agents?
losartan, valsartan, irbesartan, candesartan, telmisartan, eprosartan, olmesartan, azilsartan
adeverse effects of ACEI and ARBs
angioedema, rash, neutropenia, metallic taste, sex dysfunction, cough (not ARB), hyperkalemia, orthostatic hypotension, hypotension is also using diuretic
patient populations where ACEI or ARBs are a good choice
diabetes, renal insufficiency, acute coronary syndromes, post MI, cerebrovascular disease, CHF, work better in Caucasians than AA
patient populations where ACEI and ARBs are contraindicated
pregnancy, past angioedema, bilateral renal artery stenosis, concurrent K sparing diuretics or K supplements
why should ACEI not be used by those taking NSAIDS?
they will cause decreased blood flow to the kidneys because NSAIDS will inhibit PG and cause vasoconstriction of vessels to kidneys and ACEI will cause vasodilation of vessels leaving kidneys
what should be monitored when patients are on ACEI or ARB
BP, SCr (may increase transiently but will normalize in 2 weeks), BUN, K SE
direct renin inhibitor
Aliskiren (tekturna) 150-300mg also Tekturna HCT (combo with HCTZ)
precautions with aliskiren use
renal insufficiency, hyperkalemia, angioedema
counseling points for aliskiren
take with full glass of water, avoid high fat meals as this will decrease absorption, avoid during pregnancy
calcium channel blockers MOA
MOA= blocks inward movement of Ca across cell membranes, relaxes smooth muscle
nondihydropyridines, cause vasodilation, depress cardiac contractility, inhibit AV conduction
cardioselective CCB agents
vasoselective CCB agents
dihydropyridines, nifedipine, nicardipine, isradipine, felodipine, amlodipine, nisoldipine, clevidipine
adverse effects of nondihydropyridines
some peripheral edema, bradycardia, orthostatic hypotension, constipation (verapamil), AV conduction disturbances
patient populations that CCB work well
geriatrics, African Americans, IHD
populations to avoid CCB
GERD, CHF (can use amlodipine or felodipine, dihydropyridines will cause edema, verapamil/diltiazem will decrease HR and CO)
drug interactions of CCB
verapamil>diltiazem inhibits 3A4, use with cautions with B blockers due to heart block, caution with grapefruit juice
stimulation of alpha 1 receptors will cause....
vasoconstriction...thus an alpha 1 receptor blocker will cause vasodilation
stimulation of beta 1 will cause.....
increase in HR and force...thus a beta1 receptor blocker will cause a decrease in HR ....decrease in CO....decrease in BP
stimulation of beta 2 will cause....
Beta blockers/alpha-beta blockers MOA
MOA=blocke beta receptors.....decrease HR, decrease CO, increase TPR
beta blocker agents
atenolol, bisoprolol, betaxolol, metoprolol, nebivolol, nadolol, propranolol, timolol, acebutolol, penbutolol, pindolol, labetalol, carvedilol
what types of B blockers are preferred in asthma, PVD and DM?
B 1 selective
what types of B blockers are preferred in patients with bradycardia?
those with Intrinsic sympathomimetic activity
what types of B blockers shoud be avoided in those with migraines and angina?
those with Intrinsic sympathomimetic activity
some SE of B blockers
fatigue, insomnia, bizarre dreams, sex dysfunction, decreased exercise tolerance
what should be monitored when on B blockers
BP, HR, lipid profile, SE
peripheral alpha 1 antagonists MOA
MOA= blocks post-synaptic alpha 1 receptors leading to vasodilation, decreased BP (preload and afterload reducers)
peripheral alpha 1 antagonist agents
prazosin, terazosin, doxazosin
SE of peripheral alpha 1 blockers
1st dose syncope, dizziness, weakness, HA, reflex tachycardia, Na/H2O retention, priapism, icreases HDL, decreases LDL
*=not an adverse effect
when should peripheral alpha 1 blockers be taken?
dose at HS
which patient populations do well on alpha 1 blockers?
those with BPH, those with hyperlipidemia
which patient population should avoid alpha 1 blockers?
elderly.....risk of falls
central alpha 2 agonists MOA
MOA= stimulates alpha receptors in the CNS inhibiting sympathetic outflow to the heart, kidneys and periphery....decrease in BP
central alpha 2 agonist agents
methyldopa, clonidine, guanabenz, guanfacine
patient counseling points when using clonidine patch
leave patch on for 7 days, rotate sites non hairy, non shaved
how do you switch a patient from PO clonidine to clonidine patch?
day1-place patch and 100% of oral dose, day 2-50% of oral dose, day 3-25% of oral dose, day 4-no PO dose
clonidine patch strengths
TTS-1 is 0.1mg/24hr clonidine, TTS-2 is 0.2mg/24hr clonidine, TTS-3 is 0.3mg/24hr clonidine
adeverse effects of central alpha 2 agonists
orthostatic hypotension, sedation, dizziness, xerostomia, Na/H2O retention, sex dysfunction, hemolytic anemia, fatigue, rebound HTN, depression, increased LFT (methyldopa)
which antihypertensive agent can also be used for menopause symptoms?
which antihypertensive agent can also be used for smoking cessation?
which antihypertensive agents can be used in ADHD associated tics?
what is the central alpha 2 agonist preferred in pregnancy?
adrenergic agonist MOA
MOA= inhibit catecholamine release from peripheral sites....decreased HR and decrease BP
adrenergic agonist agent
adverse effects of reserpine
orthostatic hypotension, diarrhea, sex dysfunction, nasal congestion, depression, sedation , fatigue, bradycardia, Na/H2O retention
direct vasodilator MOA
MOA= cause direct vasodilation of arterial smooth muscle
direct vasodilator agents
T or F: direct vasodilators should be given as monotherapy
FALSE: they should be given with B blocker and diurectic
what is one important SE of direct vasodilators?
if patient is coming off of clonidine and B blocker, which should be d/c'd first?
taper and d/c B blocker, then taper and d/c clonidine
which antihypertensives can cause rebound HTN and should therefore be tapered?
central alpha 2 agonists (clonidine) and B blockers...taper over 4-5 days
T or F: BP meds may be stepped down if BP is stable
TRUE: if BP is under stable control for 6-12 months we can decrease the dosage or the # of drugs
what antiHTN should be avoided in DM?
what antiHTN should be avoided in asthma/COPD?
what antiHTN should be avoided in hyperlipidemia?
BB w/o ISA, diuretics(use with caution)
what antiHTN should be avoided in PVD?
what antiHTN should be avoided in CHF?
CCB, nonselective BB
what antiHTN should be avoided in IHD?
direct vasodilators (hydralazine and minoxidil)
T or F: diruetics are the best agent to use in gout
FALSE: use diuretics with caution in gout and hyperurecemia
what are the best antiHTN to use in renal insufficiency?
metolazone, loops, ACEI, ARBs, hydralazine
what are the best antiHTN agents to use in a patient who has tachycardia?
BB w/o ISA, cardioselective CCB
what antiHTN can exacerbate GERD?
what antiHTN can cause gynecomastia?
spironolactone....thus good for hyperaldosteronism
what antiHTN agent should be used in someone with tremor?
what are some good agents to use in patients with migraines?
CCB (verapamil), BB(non ISA and lipid soluble), clonidine
which antiHTN should be avoided in pregnancy?
ACEI, ARBs, aliskiren (teratogenic), CCB( can cause contractions in 3rd trimester)
what antiHTN are the best for use in peds?
ACEI, BB and diuretics